Testosterone (T) exerts anxiolytic effects through functional androgen receptors (ARs) in rodents. T treatment of castrated mice reduces anxiety-like behavior in wild-type (WT) males, but not males with a spontaneous mutation that renders AR dysfunctional (testicular feminization mutation, Tfm). Using Cre-LoxP technology we created males carrying induced dysfunctional AR allele (induced TFM; iTfm) to determine the brain regions responsible for T-induced anxiolysis. Adult WT and iTfm mice were castrated and T treated. Castrated WTs given a blank capsule (WT + B) served as additional controls. Mice were later exposed to the anxiogenic light/dark box, sacrificed and their brains processed for immediate early gene cFos immunoreactivity. Analyses revealed that T treatment increased cFos-expressing neurons in the basolateral amygdala (blAMY) of WT males, but not in iTfm males, which did not differ from WT + B mice. In contrast, WT + T males displayed fewer cFos + cells than iTfm + T or WT + B groups in the suprachiasmatic nucleus of the hypothalamus (SCN). No effects of genotype or hormone were seen in cFos expression in the hippocampus, medial prefrontal cortex, paraventricular nucleus of the hypothalamus, oval and anterodorsal bed nucleus of the stria terminalis, or dorsal periaqueductal grey. AR immunohistochemistry indicated that ∼65 % of cells in the blAMY and SCN were AR + in WT males, so AR could act directly within neurons in these regions to modulate the animals' response to anxiogenic stimuli. Because absence of a functional AR did not affect cFos response to mild stress in the other brain regions, they are unlikely to mediate androgen's anxiolytic effects. Neonatal hypoxia-ischemia (HI) is one of the commonest conditions which seriously influences the development of infants' nervous system and causes series of neurological sequelaes. The aim of the present study was to analyze the potential regulatory mechanism of long non-coding (lnc) RNA H19 under hypoxia conditions. Neural stem cells (NSCs) were incubated in hypoxic conditions for 8 h to induce hypoxia injury. qRT-PCR was performed to detect H19 or micro (miR)-107 expression. Cell Counting Kit-8 (CCK-8) assay and Annexin V-FITC/PI staining assay were employed to detect the effects of hypoxia on cell viability and apoptosis, respectively. Moreover, NSCs were transfected with H19 overexpressing plasmid or shRNA-H19 and then subjected to hypoxia treatment. The effects of H19/miR-107 on NSC cell biological behaviors were confirmed. Furthermore, the signaling pathways involved in HI were analyzed using western blot. Hypoxia treatment restrained cell viability and induced cell apoptosis in NSCs. Overexpression of lncRNA H19 attenuated hypoxia-induced NSCs injury, while knockdown of lncRNA H19 aggravated NSCs injury. Further experiments suggested that miR-107 up-regulation reversed the effects of lncRNA H19 overexpression on NSCs. Moreover, the activation of Wnt/β-catenin and PI3K/AKT pathways triggered by H19 were reversed by miR-107 up-regulation in hypoxia-treated NSCs. LncRNA H19 overexpression attenuated hypoxia-induced NSCs injury and promoted activation of Wnt/β-catenin and PI3K/AKT pathways through downregulating miR-107. LncRNA H19 overexpression attenuated hypoxia-induced NSCs injury and promoted activation of Wnt/β-catenin and PI3K/AKT pathways through downregulating miR-107.Physical inactivity is positively associated with anxiety and depression. Considering physical inactivity, anxiety, and depression each have a genetic basis for inheritance, our lab used artificial selectively bred low-voluntary running (LVR) and wild type (WT) female Wistar rats to test if physical inactivity genes selected over multiple generations would lead to an anxiety or depressive-like phenotype. We performed next generation RNA sequencing and immunoblotting on the dentate gyrus to reveal key biological functions from heritable physical inactivity. LVR rats did not display depressive-like behavior. However, LVR rats did display anxiogenic behavior with gene networks associated with reduced neuronal development, proliferation, and function compared to WT counterparts. Additionally, immunoblotting revealed LVR deficits in neuronal development and function. To our knowledge, this is the first study to show that by selectively breeding for physical inactivity genes, anxiety-like genes were co-selected. The study also reveals molecular insights to the genetic influences that physical inactivity has on anxiety-like behavior. In a hospital setting, there is a need for rapid detection of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) to guide isolation measures and targeted admission. To evaluate the diagnostic performance of five SARS-CoV-2 rapid nucleocapsid protein antigen detection (RAD) assays (Biosynex, Biotical, Orient Gene, Panbio and SD Biosensor), and describe the performance and impact of implementation of the SD Biosensor assay in an emergency department. Sensitivity and specificity of the five RAD assays were analysed on 100 respiratory samples 60 real-time reverse transcriptase polymerase chain reaction (rRT-PCR)-confirmed SARS-CoV-2-positive samples, 24 SARS-CoV-2 RNA-negative samples and 16 samples positive for other respiratory pathogens. The manufacturer's protocol was adapted to validate the antigen tests on transport media used for rRT-PCR in the authors' routine practice. The SD Biosensor RAD assay was implemented as a screening method for rapid diagnosis and targeted admission. Sensitivitargeted admission.Non-degradable plastics such as polyethylene (PE), polypropylene (PP), polystyrene (PS), and polyethylene terephthalate (PET) are among the most generated plastic wastes in municipal and industrial waste streams. The mismanagement of abandoned plastics and toxic plastic additives have threatened marine and land fauna as well as human beings for several decades. https://www.selleckchem.com/products/SRT1720.html The available thermal processes can degrade plastic at pilot- and commercial-scale. However, they are energy-intensive and can generate toxic gases. Degradation of plastic waste with the help of live microorganisms (biodegradation) is an eco- and environmentally friendly method for plastic degradation, although the slow processing time and low degradation rate still hinder its applications at pilot- and large-scale. In this review, the advantages and limitations of current plastic degradation methods, their technology readiness levels (TRL), biodegradation mechanisms and the associated challenges in biodegradation are assessed in detail. Based on this analysis, a path toward an efficient and greener way toward degradation of non-recyclable single-use PE, PP, PS and PET plastic is proposed.